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SUMMARY:Modeling of cardiac Ischemia in human myocytes and tissue includin
 g spatiotemporal electrophysiological variations - Seemann\, G (Karlsruhe 
 (TH))
DTSTART:20090723T150000Z
DTEND:20090723T151500Z
UID:TALK19155@talks.cam.ac.uk
CONTACT:Mustapha Amrani
DESCRIPTION:Cardiac tissue exhibits spatially heterogeneous electrophysiol
 ogical properties. In cardiac diseases\, these properties change also in t
 ime. This study introduces a framework to investigate their role in cardia
 c ischemia using mathematical modeling and computational simulations at ce
 llular and tissue level. Ischemia was incorporated by reproducing effects 
 of hyperkalemia\, acidosis\, and hypoxia with a human electrophysiological
  model. In tissue\, spatial heterogeneous ischemia was described by centra
 l ischemic (CIZ) and border zone. Anisotropic conduction was simulated wit
 h a bidomain approach in an anatomical ventricle model including realistic
  fiber orientation and transmural\, apico-basal\, and interventricular ele
 ctrophysiological heterogeneities. A model of electrical conductivity in a
  human torso served for ECG calculations. Ischemia raised resting but redu
 ced peak voltage\, action potential duration and upstroke velocity. These 
 effects were strongest in subepicardial cells. In tissue\, conduction velo
 city decreased towards CIZ but effective refractory period increases. At 1
 0 min of ischemia 19% of subepi- and 100% of subendocardial CIZ cells acti
 vated with a delay of 34.67.8 ms and 55.918.8 ms\, respectively\, compared
  to normal. Significant ST elevation and premature T wave end appeared onl
 y with the subepicardial CIZ. The model reproduced effects of ischemia at 
 cellular and tissue level. The results suggest that the presented in-silic
 o approach can complement experimental studies e.g. in understanding the r
 ole of ischemia or the onset of arrhythmia.
LOCATION:Seminar Room 1\, Newton Institute
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